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Updated: Dec 21, 2025
Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Left Ventricular Extracellular Volume Expansion Is Not Associated with Atrial Fibrillation or Atrial
Suvai Gunasekaran1, Daniel C Lee1, Bradley P Knight1
1Department of Biomedical Engineering, Northwestern University, Evanston, Ill (S.G., L.F., D.K.); Department of Radiology (S.G., L.F., J.D.C., J.C.C., D.K.) and Division of Cardiology, Internal Medicine (D.C.L., B.P.K., R.P.), Northwestern University Feinberg School of Medicine, 737 N Michigan Ave, Suite 1600, Chicago, IL 60611; Department of Radiology, Mayo Clinic, Rochester, Minn (J.D.C.); and Cardiovascular MR R&D, Siemens Healthcare, Chicago, Ill (K.C.).
Insights
Left ventricular (LV) extracellular volume (ECV) expansion is not linked to atrial fibrillation (AF) or AF-related LV systolic dysfunction (LVSD). This study found no significant difference in ECV among patient groups, suggesting no association.
Area of Science:
- Cardiology
- Radiology
- Biomedical Imaging
Background:
- Atrial fibrillation (AF) is a common arrhythmia.
- Left ventricular systolic dysfunction (LVSD) can be associated with AF.
- Left ventricular (LV) extracellular volume (ECV) expansion may indicate myocardial fibrosis, potentially contributing to cardiac dysfunction.
Purpose of the Study:
- To investigate the association between LV ECV expansion and AF.
- To determine if LV ECV expansion is linked to AF-mediated LVSD.
- To minimize confounding factors in biologic and imaging methods.
Main Methods:
- Cardiovascular MRI was used to assess LV ECV in 137 AF patients and 32 controls.
- An arrhythmia-insensitive-rapid (AIR) T1 mapping sequence minimized imaging confounders.
- Biologic confounders were controlled by excluding severe LV hypertrophy and standardizing ECV measurements.
Main Results:
- No significant difference in mean LV ECV was observed between patients with AF (normal LVEF or LVSD) and controls.
- A significant interaction between ECV and CHA2DS2-VASc score was noted (P = .045).
- Nearly all AF patients (99.3%) had ECV below the fibrosis cutoff, even with low CHA2DS2-VASc scores.
Conclusions:
- LV ECV expansion is not associated with AF or AF-mediated LVSD.
- The findings suggest that myocardial fibrosis, as measured by ECV, may not be a primary driver of AF or associated LVSD in this cohort.
- Further research may explore other mechanisms underlying AF and LVSD.
Purpose:
To determine whether left ventricular (LV) extracellular volume (ECV) expansion is associated with atrial fibrillation (AF) or AF-mediated LV systolic dysfunction (LVSD) while minimizing the influence of biologic and imaging methodologic confounders.
Materials And Methods:
This study examined the prevalence of LV ECV expansion in 137 patients with AF (mean age, 62 years ± 11 [standard deviation]; 92 male patients and 45 female patients; 83 paroxysmal and 54 persistent) who underwent preablation cardiovascular MRI. Biologic confounders were minimized by measuring the ECV fraction and excluding patients with severe LV hypertrophy, defined as wall thickness greater than 1.5 cm. Imaging confounders were minimized by using an arrhythmia-insensitive-rapid (AIR) cardiac T1 mapping pulse sequence. Other cardiac functional parameters, including LV ejection fraction (LVEF) and left atrial end-diastolic volume indexed to body surface area, were assessed using cine cardiovascular MRI. A substudy was conducted in 32 patients with no AF (mean age, 54 years ± 16) in sinus rhythm to establish control values and convert these values between the AIR sequence and literature-based modified Look-Locker inversion recovery (MOLLI) values.
Results:
The mean ECV was not significantly different (P > .05) between patients with AF with a normal LVEF (24.5% ± 2.8; n = 107), patients with AF with LVSD (24.5% ± 2.5; n = 30), and patients with no AF (24.4% ± 3.8; n = 32), but there was a significant interaction between ECV and CHA2DS2-VASc score (P = .045). Compared with the literature data obtained from healthy control patients scanned using MOLLI, 99.3% of patients with AF had ECV below the fibrosis cutoff point (32.8% when converted from MOLLI T1 mapping to AIR T1 mapping), including a subset of patients with AF (n = 28) with low CHA2DS2-VASc score (0/1 for men/women).
Conclusion:
Study results suggest that an LV ECV expansion is not associated with AF or AF-mediated LVSD. Supplemental material is available for this article. © RSNA, 2020See also the commentary by Stillman in this issue.
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